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PubMed1996

Neuronal degeneration in rat cerebrocortical and olfactory regions during subchronic "binge" intoxication with ethanol: possible explanation for olfactory deficits in alcoholics.

Severe, repetitive ("binge") ethanol intoxication in adult rats (intragastric delivery 3 times daily for 4 days in a modification of the Majchrowicz method) precipitates neuronal degeneration in selected cerebral cortical regions involved in memory and olfaction, confirming the results of Switzer and colleagues (Anat. Rec. 202: 186a, 1982). Neuronal damage was visualized with the de Olmos cupric silver technique for degenerating neurons and processes (argyrophilia), and was quantitated by total counts and densities of argyrophilic cells/fields. The specificity of the degeneration provides a neuropathological basis for the olfactory memory deficits in chronic alcoholics. In highly intoxicated rats, argyrophilia was most extensive among hippocampal dentate gyrus granule cells, pyramidal neurons in layer 3 of the entorhinal cortex, and olfactory nerve terminals in the olfactory bulb. Degenerating pyramidal neurons were also consistently seen in the insular cortex and olfactory cortical regions, such as the piriform and perirhinal cortices. There were few argyrophilic neurons in the CA regions of the hippocampus and none in the cerebellum--regions generally shown to have cell loss in long-term ethanol feeding models--but degenerating mossy fibers in the CA2 region were observed. Degeneration was maximal before the peak period of abstinence symptoms in this model, because argyrophilic densities were no greater 36 hr, compared with 8 hr after the last ethanol dose. High blood ethanol levels were required, because argyrophilia, absent from isocaloric controls, also was only evident in ethanol-intoxicated rats with mean blood ethanol levels for days 2 to 4 above 300 mg/dl; however, it increased substantially between 350 and 550 mg/dl. The resemblance of the argyrophilic distribution to the regional neuropathology that occurs in experimental seizures indicates that the ethanol-induced degeneration may have an excitotoxic basis. Progressive reductions in the seizure threshold (e.g., kindling phenomena that have been documented during binge ethanol intoxication) might be associated with excitotoxic hyperactivity during the repetitive nadirs between high blood and brain ethanol peaks. However, direct toxic actions of ethanol or its metabolites could also be involved. Overall, the model should be useful for studying mechanisms of ethanol-induced selective cortical and olfactory brain damage.

Alcoholic Intoxication↗
PubMed1997

Identification and localization of dopamine receptor subtypes in rat olfactory mucosa and bulb: a combined in situ hybridization and ligand binding radioautographic approach.

Olfactory bulb (OB) of mammals contains a large population of dopaminergic interneurons within the glomerular layer. Dopamine has been shown in vivo to modulate several aspects of olfactory information processing. The dopamine receptors of olfactory bulb and mucosa are assessed here at the levels of mRNAs and radioligand binding sites with presently available tools. D1A mRNA was found in OB glomerular-, plexiform-, mitral-cell and granular layers, but not in olfactory mucosa. D1B mRNA was absent in olfactory bulb and mucosa. D1-like binding sites were detected with two distinct radioligands, in glomerular-, plexiform-, mitral cell- and granular layers of OB but not in olfactory mucosa. We thus demonstrate the previously doubtful presence of D1-like receptors in OB. D2 mRNAs were localized in the glomerular and granular layers of OB and in olfactory mucosa; lesser amounts of D3 mRNAs were found in OB glomerular and granular layer, but not in olfactory mucosa. No D4 mRNA was detected in either structure. High densities of D2-like, [125I]Iodosulpride-labelled binding sites, were revealed within lamina propria of olfactory mucosa, and confirmed in the olfactory nerve- and glomerular layers of OB. A faint but significant density of [3H]7-hydroxy-dipropyl-aminotetralin (OH-DPAT) labelled, D3 binding sites was detected in olfactory nerve- and glomerular layers of OB, but not in olfactory mucosa. Competition of [125I]Iodosulpride specific binding by three D2/D3 selective drugs yielded kinetics typical of the D2 receptor subtype in olfactory bulb and mucosa. Olfactory nerve- and glomerular layers of OB are proved thus to contain a predominant contingent of D2 receptors and a minor population of D3 receptors, while olfactory mucosa expresses only D2 receptors.

Animals↗
PubMed2005

Changes in reelin expression in the mouse olfactory bulb after chemical lesion to the olfactory epithelium.

To explore the functional roles of Reelin in the adult olfactory system, we examined changes in the expression of reelin mRNA and Reelin protein in the olfactory bulb (OB) of adult mice after a chemical lesion to the olfactory epithelium. Following intranasal irrigation with 2% zinc sulphate solution, animals were perfused at various times between 5 and 40 days post-lesion. The expression of reelin mRNA in mitral cells in the OB was slightly reduced at 5 days post-lesion, completely abolished by 20 days, but restored almost to the normal level at 40 days post-lesion. Similarly, the expression of Reelin protein in mitral cells of the deafferented OB also recovered, although not to the normal level. No recovery of either reelin mRNA or Reelin immunoreactivity was seen in the periglomerular cells and external tufted cells. The expression profile of reelin mRNA and Reelin protein in the OB coincided with the time course of degeneration and regeneration of olfactory nerves, as indicated by anterograde labeling of olfactory nerves with WGA-HRP. These results suggest that expression of reelin mRNA in the adult OB is regulated by olfactory inputs.

Animals↗
PubMed1991

Neonatal capsaicin treatment impairs functional properties of primary olfactory afferents in the rat.

Long-lasting influences of neonatal capsaicin treatment on functional properties of the olfactory nerve were studied in 30-day-old rats by determining excitability thresholds of nerve fibres by means of orthodromic field potentials elicited in the main olfactory bulb, as well as by analyzing the pattern of the low-frequency component of the bulbar electroencephalogram. In addition, body, brain and olfactory bulbar weights were measured. Neonatal capsaicin resulted in reduced excitability of primary olfactory afferents and reduced wave amplitude of the bulbar electroencephalogram. Capsaicin treated animals had reduced body, brain and bulbar weights, the latter being the most affected. The result indicates that capsaicin given early in life leads to altered transmission properties of olfactory nerve fibres at later age, suggesting that olfactory afferents are sensitive to the neurotoxic action of capsaicin as occurs in other chemosensory afferent systems.

Animals↗
PubMed1988

Postmitotic, postmigrational expression of tyrosine hydroxylase in olfactory bulb dopaminergic neurons.

The developmental expression of tyrosine hydroxylase (TOH) was studied in a large, specific population of dopaminergic (DA) neurons in the main olfactory bulb (MOB) of the rat. These DA neurons comprise an anatomically distinctive population that has been well characterized in the adult hamster (Davis and Macrides, 1983) and rat (Halasz et al., 1981; Baker et al., 1983, 1984). We addressed a basic question in developmental neurobiology: What factors regulate the expression of neuronal transmitter phenotype during development? Olfactory bulb DA neurons are born in the ventricular and subependymal zones and migrate through all intervening layers to the most superficial layer in the bulb (Altman, 1969; Bayer, 1983). The time of TOH expression in these neurons was determined using immunohistochemistry and light microscopic image-analysis techniques. The results indicate that TOH phenotype is not expressed when the cells are born in the subependymal zone nor during their migration to the periglomerular region but only after they reached their final destination, the glomerular layer. This suggests that epigenetic factors associated with the glomeruli initiate the expression of the key transmitter synthesizing enzyme in these neurons. Primary olfactory neurons in the nasal epithelium project exclusively to glomeruli of the MOB; removal of this input in adult rats (Kawano and Margolis, 1982; Baker et al., 1983, 1984), mice (Nadi et al., 1981; Baker et al., 1983), dogs (Nadi et al., 1981), and hamsters (Kream et al., 1984) appears to down-regulate the expression of the TOH in periglomerular cells. The present results suggested that the input from the primary olfactory nerve is also necessary for the initial expression of the TOH phenotype. In support of this notion, we found that lesions of the olfactory nerve during the first postnatal week caused a significant reduction in the number of TOH-positive juxtaglomerular neurons in the following weeks. Thus, the olfactory nerve appears to be necessary for both the initiation and maintenance of TOH expression in olfactory bulb neurons. These findings suggest that specific cell-cell interactions play a key role in CNS neuronal transmitter phenotype regulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Orthodromic synaptic activation of rat olfactory bulb mitral cells in isolated slices.

Axons of olfactory receptor neurons terminate in the glomerular layer of the olfactory bulb, where they synapse with the apical dendrites of mitral cells. Although the mitral cell and its excitation by the olfactory nerve have been the subject of numerous experimental investigations, in vitro studies of these neurons have primarily used nonmammalian preparations. We have recorded the responses of rat olfactory bulb mitral cells to stimulation of the olfactory nerve layer in vitro using extracellular and whole cell patch techniques. Olfactory bulbs were cut into 400-microns thick slices in approximately horizontal section and submerged in a recording chamber. Patch clamp electrodes were guided into the mitral cell layer, which was visible under a dissecting microscope. A stimulating electrode was placed onto the olfactory nerve layer (ONL) rostral to the recording electrode. In extracellular recordings, mitral cells typically responded to ONL stimulation with a prolonged excitation lasting 1 s or longer. With whole cell patch recordings, membrane resistances (mean 272 M omega) were substantially higher than those reported in previous intracellular studies that used sharp electrodes. Small spontaneous excitatory potentials were present in some mitral cells. ONL stimulation caused a prolonged depolarization comparable to the duration of the period of excitation observed in extracellular recordings. At membrane potentials near -55 mV, ONL stimulation evoked a train of spikes. All but the first of these spikes were blocked by hyperpolarization of the membrane to -65 mV.

Action Potentials↗
PubMed1995

Regeneration of olfactory sensory neurons and reconnection in the aging hamster central nervous system.

Olfactory neuron recovery and axon growth was studied in 12-24 month old hamsters after unilateral olfactory nerve transection. At recovery times ranging from 4 to 126 days olfactory nerve regeneration and axon reconnection to the olfactory bulb were examined by anterograde horseradish peroxidase (HRP) neurohistochemistry and electron microscopy. Nerve transection produced immediate retrograde neuron degeneration and there was no HRP reaction product in the bulb at 4 days post transection. By day 35, centrally growing olfactory axons had reached the bulb. Axons formed glomeruli smaller than those in the unoperated control bulb and they were not always confined to the glomerular layer of the bulb. Some animals showed robust fiber growth with axon fascicles penetrating the different layers of the bulb and forming ectopic glomeruli along their path. Second order bulb neurons contained wheat germ agglutinin HRP reaction product, indicating that transneuronal transport had occurred. Electron microscopy confirmed transneuronal transport between olfactory axons and second order bulbar neurons. These results show that the capacity for olfactory neuron recovery and reconnection persists in the hamster well into old age.

Aging↗
PubMed1980

The response of ornithine decarboxylase during neuronal degeneration and regeneration in olfactory epithelium.

Mature olfactory neurons are continually replaced from a population of progenitor cells. Olfactory nerve section, bulbectomy, or treatment with certain chemicals induces degeneration of olfactory neurons followed in some cases by regeneration. Ornithine decarboxylase (ODC) activity was measured in mouse olfactory tissues as an indicator of cellular regeneration. ODC activity in olfactory tissue (0.2-0.4 nmol/mg protein/h) is 10-30 times higher than in a variety of other cerebral tissues. Within 3 h after unilateral olfactory nerve section, ODC activity in the epithelium declines to 50% of control followed by a slow return to basal activity by 6 days. In the same animals, ODC activity increases severalfold in bulb (1 day) with a gradual decline to normal (9 days). Except for an early transient increase, the effects of unilateral bulbectomy on epithelial ODC activity are similar to those seen after nerve section. The changes in ODC activity following intranasal irrigation with 10 mM-colchicine also closely mimic those seen after nerve section. The effects of intranasal irrigation on ODC activity with 0.5% Triton X-100 or 0.17 M-ZnSO4 are more complex. Thus, when the mature neuronal population is degenerating after surgery or chemical treatments, ODC activity decreases in the epithelium. The subsequent increase of ODC activity prior to reconstitution of the mature neuronal population probably reflects the regeneration mechanism of the olfactory epithelium. The increase of ODC activity in the olfactory bulb after nerve section is best interpreted as a cellular injury response. These alterations in ODC activity in olfactory tissues after chemical and surgical treatments constitute the earliest biochemical events observed in these tissues in response to cellular damage.

Aging↗
PubMed1996

Glycosaminoglycans in the olfactory epithelium and nerve of chick embryos: an immunocytochemical study.

Immunoreactivity specific to keratan sulfate (KS), heparan sulfate (HS), and chondroitin sulfate (CS) in the nasal region of chick embryos on embryonic day (ED) 3.5-7, was investigated with six antibodies and three glycosidases. Immunoreactivity specific to HS, KS, and CS, and their localized distribution was seen in the olfactory epithelium, olfactory nerve, and cells located along the bundles of the olfactory nerve on ED 3.5-7. The immunoreactivity to HS was seen in the cells and their neurites located in the olfactory nerve bundles and in cells in the ventral forebrain on ED 3.5-5. The cells, i.e., gonadotropin-releasing hormone (GnRH)-or somatostatin-containing cells, are reported to originate in the olfactory epithelium, migrate along the olfactory nerve, and then invade the forebrain in chick embryos. These findings taken together, indicated that a subset of cells migrating along the nerve to the forebrain contained HS. Limited immunoreactivity to KS in the olfactory epithelium and in the underlying mesenchyme, but not in the olfactory nerve, ruled out the involvement of this glycosaminoglycan (GAG) in the migration of cells along the olfactory nerve. The immunoreactivity to CS and to its derivatives suggested the presence of CS in proteoglycan form in the olfactory structures and migrating cells.

Animals↗
PubMed1982

Structure of the mitral cell in the olfactory bulb of the goldfish (Carassius auratus).

The mitral cell in the olfactory bulb of the goldfish was examined by means of light microscopy, high-voltage electron microscopy, and conventional electron microscopy. Mitral cells are located rather diffusely throughout the glomerular and plexiform layers. They do not make their own discrete layer. The cell bodies are rounded or triangular, and are about 10-25 micrometers in diameter. In Golgi-impregnated material, thick cylindrical dendrites can be seen arising from the cell bodies and branching in the glomerular layer. Dendritic branches of some cells make two or more rather compact tufts, while the dendrites of other cells intermingle loosely with one another. In semithin and thin sections, darkly stained nodules appear to be scattered diffusely in the glomerular layer without clustering into discrete spheres, which are characteristic of the mammalian glomerulus. Hence, instead of the glomerulus, the "glomerular area" is defined as an area consisting of darkly stained nodules with rather pale granular regions surrounding them. Branches of mitral cell dendrites in the glomerular area consist of cylindrical shafts and irregular appendages arising from them. The shafts appear in the pale granular region and the appendages are found in the darkly stained nodules. Synapses can be found on all parts of the mitral cell: the soma, axon hillock, axon initial segment, thick dendritic stems, and dendritic branches. The abundance of synapses seems to vary considerably from part to part, and is highest on the dendritic branches in the glomerular area. The mitral cell is postsynaptic to olfactory nerve terminals and granule cell dendrites, and presynaptic to granule cell dendrites and some processes of unknown origin. Olfactory nerve terminals make asymmetrical synapses specifically on the appendages of the dendritic branches. Of the synapses on the shafts of the mitral cell dendritic branches in the glomerular area, 90% are with granule cell dendrites. Of the synapses between two different kinds of processes 30% are mitral-to-granule asymmetrical synapses, 20% are granule-to-mitral symmetrical synapses, and 50% are reciprocal pairs. Gap junctions and mixed synapses are also seen on branches of mitral cell dendrites. Features of the goldfish mitral cell are compared with those of the mammal. The differences in neuronal organization between the olfactory bulbs of teleosts and mammals are discussed.

Animals↗
PubMed2006

Implantation of a scaffold following bulbectomy induces laminar organization of regenerating olfactory axons.

Primary olfactory axons expressing different odorant receptors are interspersed within the olfactory nerve. However, upon reaching the outer nerve fiber layer of the olfactory bulb they defasciculate, sort out, and refasciculate prior to targeting glomeruli in fixed topographic positions. While odorant receptors are crucial for the final targeting of axons to glomeruli, it is unclear what directs the formation of the nerve fiber and glomerular layers of the olfactory bulb. While the olfactory bulb itself may provide instructive cues for the development of these layers, it is also possible that the incoming axons may simply require the presence of a physical scaffold to establish the outer laminar cytoarchitecture. In order to begin to understand the underlying role of the olfactory bulb in development of the outer layers of the olfactory bulb, we physically ablated the olfactory bulbs in OMP-IRES-LacZ and P2-IRES-tau-LacZ neonatal mice and replaced them with artificial biological scaffolds molded into the shape of an olfactory bulb. Regenerating axons projected around the edge of the cranial cavity at the periphery of the artificial scaffold and were able to form an olfactory nerve fiber layer and, to some extent, a glomerular layer. Our results reveal that olfactory axons are able to form rudimentary cytoarchitectonic layers if they are provided with an appropriately shaped biological scaffold. Thus, the olfactory bulb does not appear to provide any tropic substance that either attracts regenerating olfactory axons into the cranial cavity or induces these axons to form a plexus around its outer surface.

Animals↗
PubMed2005

The olfactory organ modulates gonadotropin-releasing hormone types and nest-building behavior in the tilapia Oreochromis niloticus.

Direct olfactory inputs to any of the known gonadotropin-releasing hormone (GnRH) containing neurons have not been demonstrated. Therefore, the rationale of this study was to examine whether olfactory inputs might in some way interact with the GnRH system(s) to synchronize reproductive behaviors. In order to establish this, we used anosmic mature male tilapia to investigate changes in reproductive behaviors, gonadal morphology, and GnRH1, GnRH2, and GnRH3 cellular morphology and change in GnRH mRNA levels by real-time polymerase chain reaction. Bilateral removal of the olfactory rosettes followed by occlusion of the nasal cavity (ORX) inhibited nest-building behavior, but had no effect on aggressive and sexual behaviors or gonadal morphology. ORX failed to alter the morphological features of GnRH1, GnRH2, and GnRH3 (cell number, size, GnRH optical density), but significantly decreased copies of GnRH1 and GnRH2 mRNAs. GnRH immunoreactive fibers were not evident in the olfactory nerve and rosettes. DiI application to the olfactory nerve labeled inputs primarily to the glomerular layer of the olfactory bulbs and extrabulbar inputs to the forebrain but not to GnRH neurons. These results provide evidence that the olfactory rosette is crucial for modulating nest-building behavior through second-order olfactory pathways interacting with GnRH1 and GnRH2 neuronal systems.

Aggression↗
PubMed1987

High substance P-like immunoreactivity (SPLI) in the olfactory and electrosensory cells of gymnotid fish.

Substance P has been proposed as a candidate neurotransmitter or neuromodulator in the nociceptive system. Using a light microscopial immunohistochemical peroxidase-anti-peroxidase technique we have detected high substance P-like immunoreactivity (SPLI) in several types of sensory organs of 4 species of gymnotiform teleost fish: olfactory epithelium, vestibular, lateral line and electrosensory organs. The olfactory nerve and its endings within the olfactory bulb and the telencephalon were also strongly labelled. At these sites no SPLI was revealed in other teleosts (Carassius auratus, Gnathonemus petersii). The findings suggest that substance P may be involved in neurotransmission or neuromodulation in these specific sensory systems of these species.

Animals↗
PubMed2001

Imaging of the olfactory system.

The olfactory system consists of the primary olfactory nerves in the nasal cavity, the olfactory bulbs and tracts, and numerous intracranial connections and pathways. Diseases affecting the sense of smell can be located both extracranially and intracranially. Many sinonasal inflammatory and neoplastic processes may affect olfaction. Intracranially congenital, traumatic, and neurodegenerative disorders are usually to blame for olfactory dysfunction. The breadth of diseases that affect the sense of smell is astounding, yet the imaging ramifications have barely been explored.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Calcium permeable AMPA receptors and autoreceptors in external tufted cells of rat olfactory bulb.

Glomeruli are functional units of the olfactory bulb responsible for early processing of odor information encoded by single olfactory receptor genes. Glomerular neural circuitry includes numerous external tufted (ET) cells whose rhythmic burst firing may mediate synchronization of bulbar activity with the inhalation cycle. Bursting is entrained by glutamatergic input from olfactory nerve terminals, so specific properties of ionotropic glutamate receptors on ET cells are likely to be important determinants of olfactory processing. Particularly intriguing is recent evidence that AMPA receptors of juxta-glomerular neurons may permeate calcium. This could provide a novel pathway for regulating ET cell signaling. We tested the hypothesis that ET cells express functional calcium-permeable AMPA receptors. In rat olfactory bulb slices, excitatory postsynaptic currents (EPSCs) in ET cells were evoked by olfactory nerve shock, and by uncaging glutamate. We found attenuation of AMPA/kainate EPSCs by 1-naphthyl acetyl-spermine (NAS), an open-channel blocker specific for calcium permeable AMPA receptors. Cyclothiazide strongly potentiated EPSCs, indicating a major contribution from AMPA receptors. The current-voltage (I-V) relation of uncaging EPSCs showed weak inward rectification which was lost after > approximately 10 min of whole-cell dialysis, and was absent in NAS. In kainate-stimulated slices, Co(2+) ions permeated cells of the glomerular layer. Large AMPA EPSCs were accompanied by fluorescence signals in fluo-4 loaded cells, suggesting calcium permeation. Depolarizing pulses evoked slow tail currents with pharmacology consistent with involvement of calcium permeable AMPA autoreceptors. Tail currents were abolished by Cd(2+) and (+/-)-4-(4-aminophenyl)-2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX), and were sensitive to NAS block. Glutamate autoreceptors were confirmed by uncaging intracellular calcium to evoke a large inward current. Our results provide evidence that calcium permeable AMPA receptors reside on ET cells, and are divided into at least two functionally distinct pools: postsynaptic receptors at olfactory nerve synaptic terminals, and autoreceptors sensitive to glutamate released from dendrodendritic synapses.

Animals↗
PubMed2001

Glucagon-like immunoreactivity in the forebrain and pituitary of the teleost, Clarias batrachus (Linn.).

The organization of glucagon-like immunoreactivity (GLI) in the olfactory system, forebrain, and pituitary was investigated in the teleost Clarias batrachus. Weak to moderate GLI was seen in some olfactory receptor neurons and basal cells of the olfactory epithelium. Intense GLI was seen in the olfactory nerve fascicles that ran caudally to the bulb, spread over in the olfactory nerve layer, and profusely branched in the glomerular layer to form tufts organized as spherical neuropils; some of the immunoreactive fibers seem to closely enfold the mitral cells. In the inner cell layer of the bulb, some granule cells were intensely immunoreactive. Although there were thick fascicles of immunoreactive fibers in the medial olfactory tracts (MOT), the lateral olfactory tracts were generally devoid of immunoreactivity. Immunoreactive fibers in the medial olfactory tract penetrated into the telencephalon from its rostral pole and entered into the area ventralis telencephali/pars ventralis where the compact fiber bundles loosen somewhat and course dorsocaudally into the area ventralis telencephali/pars supracommissuralis just above the anterior commissure. While some immunoreactive fibers decussated in the anterior commissure, fine fibers were seen in the commissure of Goldstein. Isolated immunoreactive fibers of the medial olfactory tract were traced laterally into the area dorsalis telencephali/pars lateralis ventralis and mediodorsally into the area dorsalis telencephali/pars medialis. However, a major component of the MOT continued dorsocaudally into the thalamus and terminated in the habenula. Two immunoreactive neuronal groups and some isolated cells were seen in the periventricular region of the thalamus. Although nucleus preopticus showed no immunoreactivity, some neurons of the nucleus lateralis tuberis displayed moderate GLI. Several immunoreactive cells were seen in the pars intermedia of the pituitary gland; few were encountered in the rostral pars distalis and proximal pars distalis. Immunoreactive fibers were seen throughout the pituitary gland.

Animals↗
PubMed1996

Tyrosine hydroxylase expression in rat olfactory bulb transplants: an electron microscope study.

Juxtaglomerular (JG) neurons of rat olfactory bulb (OB) have been shown to express tyrosine hydroxylase (TH), the rate-limiting enzyme in the catecholamine synthesis pathway. These JG neurons act as inhibitory dopaminergic interneurons, modulating the incoming signal from the primary olfactory afferents. The JG neurons, comprised of periglomerular, external tufted, and short axon cells, stop expressing TH after lesions of the olfactory nerve or closure of the nares, both of which cause a loss of functional input. Upon reinnervation by a continuously regenerating olfactory nerve, these cells resume their expression of TH. In order to study deafferentation and subsequent reinnervation within this system, our laboratory utilizes a transplantation model. Sections from transplant (TX) OBs are reacted for TH using immunocytochemical localization protocols and studied by light- and especially electron microscopy (EM). Autoradiography of tritiated thymidine-labeled tissue was performed to confirm donor origin of the TX OBs. Although the architecture of the TX OB is somewhat disrupted and the TH-positive cells were not as uniform in their arrangement as they are in the normal OB, we found that the TH cells in the TH OB had a morphology similar to the JG cells observed in normal OB. These TH cells were also found to receive synaptic contacts with host olfactory nerve axons as well as make and receive contacts with the processes of donor neurons. These, synaptic contacts were formed within areas that resemble the glomeruli of normal olfactory bulb, suggesting that the inhibitory synaptic pathway is reestablished within the TX OB. These findings also suggested that host olfactory axons formed a functional contact with the TH cells, possibly inducing them to express this enzyme. This study implies that the TX OB retains a level of plasticity that enables it to recapitulate part of the interneuronal arrangement observed in the normal system.

Animals↗
PubMed2000

Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb--IV. Intraglomerular synapses of tyrosine hydroxylase-immunoreactive neurons.

Synapses of intraglomerular processes of tyrosine hydroxylase-immunoreactive neurons in the rat main olfactory bulb were examined by electron microscopic immunocytochemistry. Prominent characteristics of intraglomerular synapses of tyrosine hydroxylase-immunoreactive elements were that the vast majority (about 80%) of their synaptic inputs were asymmetrical synapses from olfactory nerve terminals and, though far smaller in proportion, one half of the remaining were asymmetrical synapses from mitral/tufted cell dendrites and the other half were symmetrical synapses from gamma-aminobutyric acid-like immunoreactive elements. So far, we have observed no typical reciprocal synapses between tyrosine hydroxylase-immunoreactive processes and mitral/tufted dendrites; however, we have often identified serial synapses; that is, asymmetrical synapses from olfactory nerve terminals or mitral/tufted cell dendrites to tyrosine hydroxylase-immunoreactive processes, and then symmetrical synapses from the latter to different mitral/tufted cell dendrites. These synaptic connections of tyrosine hydroxylase-immunoreactive neurons were very different from those of Calbindin-D(28k)-immunoreactive neurons, which received no synaptic contact directly from olfactory nerve terminals but formed reciprocal synapses with mitral/tufted cells as we analysed previously.Thus, our present and previous electron microscopic studies combined with confocal laser scanning light microscopy clearly indicated for the first time the heterogeneity of periglomerular neurons, not only in their chemical and morphological features, but also in their synaptic organization in the olfactory glomerulus.

Animals↗